The biological basis of the phenotypic diversity observed in JAK2V617F-positive myeloproliferative neoplasms is poorly understood. In this issue of Cancer Cell, Chen et al. describe that interferon and STAT1 signaling are activated in essential thrombocythemia but not in polycythemia vera. STAT1 promotes megakaryopoiesis and thus contributes to an essential thrombocythemia phenotype.